Regulation of endothelial nitric-oxide synthase (NOS) S-glutathionylation by neuronal NOS: evidence of a functional interaction between myocardial constitutive NOS isoforms.

Journal article

Background

PWhether neuronal nitric-oxide synthase (nNOS) plays a role in the endothelial NOS (eNOS)-dependent negative inotropic effect of β3-adrenergic stimulation remains to be established.

Results

nNOS knock-out or inhibition leads to increased superoxide production, eNOS uncoupling, and abrogation of β3-adrenergic responses.

Conclusion

Disabling nNOS disrupts eNOS function and downstream signaling.

Significance

nNOS plays a crucial role in preserving myocardial nitroso-redox balance and coupled eNOS activity.

Authors: Idigo, W; Reilly, S; Zhang, M; Zhang, Y; Jayaram, R

• Publication status: Published
• Peer review status: Peer reviewed
• Publisher: American Society of Biochemistry and Molecular Biology
• Journal: Journal of Biological Chemistry
• Volume: 287
• Issue: 52
• Pages: 43665-43673
• Publication date: 2012-10-01
• Acceptance date: 2012-10-19
• DOI: 10.1074/jbc.m112.412031
• EISSN: 1083-351X
• ISSN: 0021-9258
• Language: English
• Keywords: Citrulline; Nitric Oxide Synthase Type I; Mice; Xanthine Dehydrogenase; Heart Ventricles; Myocytes, Cardiac; Enzyme Inhibitors; Calcium Signaling; Superoxides; Nitric Oxide Synthase Type III; NADPH Oxidase; Isoenzymes; NG-Nitroarginine Methyl Ester; Membrane Glycoproteins; Arginase; Thiourea; Receptors, Adrenergic, beta-3; Myocardium; Mice, Knockout; Muscle Proteins; Phosphorylation; Animals